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Hemostasis or haemostasis (from the Ancient Greek: αἱμόστασις haimóstasis "styptic (drug)") is a process which causes bleeding to stop, meaning to keep blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage). It is the first stage of wound healing. Most of the time this includes blood changing from a liquid to a solid state. All situations that may lead to hemostasis are portrayed by the Virchow's triad. Intact blood vessels are central to moderating blood's tendency to clot. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor which initiate the maintenance of hemostasis after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a clot that seals the hole until tissues are repaired.


Steps of mechanism

Aggregation of thrombocytes (platelets). Platelet rich human blood plasma (left vial) is a turbid liquid. Upon addition of ADP, platelets are activated and start to aggregate, forming white flakes (right vial)

Hemostasis occurs when blood is present outside of the body or blood vessels. It is the instinctive response for the body to stop bleeding and loss of blood. During Hemostasis three steps occur in a rapid sequence. Vascular spasm is the first response as the blood vessels constrict to allow less blood to be lost. In the second step, platelet plug formation, platelets stick together to form a temporary seal to cover the break in the vessel wall. The third and last step is called coagulation or blood clotting. Coagulation reinforces the platelet plug with fibrin threads that act as a “molecular glue”.[1] Platelets are a large factor in the hemostatic process. They allow for the creation the “platelet plug” that forms almost directly after a blood vessel has been ruptured. Within seconds of a blood vessel’s epithelial wall being disrupted platelets begin to adhere to the sub-endothelium surface. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes the platelet plug is completely formed by fibrin.[2] Hemostasis is maintained in the body via three mechanisms:

  1. Vascular Spasm - Damaged blood vessels constrict. Vascular spasm is the blood vessels first response to injury. The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss. This response is triggered by factors such as a direct injury to vascular smooth muscle, chemicals released by endothelial cells and platelets, and reflexes initiated by local pain receptors. The spasm response becomes more effective as the amount of damage is increased. Vascular spasm is much more effective in smaller blood vessels.[1]
  1. Platelet plug formation - Platelets adhere to damaged endothelium to form platelet plug (primary hemostasis) and then degranulate. Platelet Plug Formation: Platelets play one of the biggest factors in the hemostatic process. Being the second step in the sequence they stick together (aggregation) to form a plug that temporarily seals the break in the vessel wall. As platelets adhere to the collagen fibers of a wound they become spiked and much stickier. They then release chemical messengers such as adenosine diphosphate (ADP), serotonin and thromboxane A2. These chemicals are released to cause more platelets to stick to the area and release their contents and enhance vascular spasms. As more chemicals are released more platelets stick and release their chemicals; creating a platelet plug and continuing the process in a positive feedback loop. Platelets alone are responsible for stopping the bleeding of unnoticed wear and tear of our skin on a daily basis.[3]

The second stage of Hemostasis involves platelets that move throughout the blood. When the platelets find an exposed area or an injury, they begin to form what is called a platelet plug. The platelet plug formation is activated by a glycoprotein called the Von Willebrand factor (VWF), which are found in the body’s blood plasma. When the platelets in the blood are activated, they then become very sticky so allowing them to stick to other platelets and adhere to the injured area.[4][5]

There are a dozen proteins that travel along the blood plasma in an inactive state and are known as clotting factors. Once the platelet plug has been formed by the platelets, the Clotting factor begin creating the platelet plug. When this occurs the clotting factors begin to form a collagen fiber called fibrin. Fibrin mesh is then produced all around the platelet plug, which helps hold the fibrin in place. Once this begins, red and white blood cells caught up in the fibrin mesh which causes the clot to become even stronger.[3]

  1. Blood coagulation - Clots form upon the conversion of fibrinogen to fibrin, and its addition to the platelet plug (secondary hemostasis). Coagulation: The third and final step in this rapid response reinforces the platelet plug. Coagulation or blood clotting uses fibrin threads that act as a glue for the sticky platelets. As the fibrin mesh begins to form the blood is also transformed from a liquid to a gel like substance through involvement of clotting factors and pro-coagulants. The coagulation process is useful in closing up and maintaining the platelet plug on larger wounds. The release of Prothrombin also plays an essential part in the coagulation process because it allows for the formation of a thrombus, or clot, to form. This final step forces blood cells and platelets to stay trapped in the wounded area. Though this is often a good step for wound healing, it has the ability to cause severe health problems if the thrombus becomes detached from the vessel wall and travels through the circulatory system; If it reaches the heart or brain it could lead to stroke, heart attack, or pulmonary embolism. However, without this process the healing of a wound would not be possible.[1]

Types of Hemostasis

Hemostasis can be achieved in various other ways if the body cannot do it naturally (or needs help) during surgery or medical treatment. When the body is under shock and stress, hemostasis is harder to achieve. Though natural hemostasis is most desired, having other means of achieving this is vital for survival in many emergency settings. Without the ability to stimulate Hemostasis the risk of hemorrhaging is great. During surgical procedures the types of hemostasis listed below can be used to control bleeding while avoiding and reducing the risk of tissue destruction. Hemostasis can be achieved by chemical agent as well as mechanical or physical agents. Which hemostasis type used is determined based on the situation.[6]

Hemostasis in emergency medicine

Some main types of Hemostasis used in emergency medicine include:


Disorders can be diseases such as hemophilia where blood does not clot sufficiently, or formation of unwanted blood clots where blood clots unnecessarily. Thrombi (blood clots) can embolize and potentially cause a heart attack or pulmonary embolism, which can be fatal. Many people eventually die because of a disorder of hemostasis.

For patients with these types of hemostasis conditions hemophilia therapy is used to try and help make of for the lack of ability to form blood clots. The best thing for these people is to try and prevent themselves from bleeding. Hemophilia therapy is where the clotting factors that are missing are actually replaced via medications. Most bleedings will stop after one dose but some require multiple treatments.[11]

History of Artificial Hemostasis

The process of preventing blood loss from a vessel or organ of the body is referred to as Hemostasis. The term comes from the Ancient Greek roots "heme" meaning blood, and "stasis" meaning halting; Put together means the "halting of the blood".[1] The origin of Hemostasis dates back as far as ancient Greece; first referenced to being used in the Battle of Troy. It started with the realization that excessive bleeding inevitably equaled death. Vegetable and mineral styptics were used on large wounds by the Greeks and Romans until the takeover of Egypt around 332BC by Greece. At this time many more advances in the general medical field were developed based off the study of Egyptian mummification practice, which led to greater knowledge of the hemostatic process. It was during this time that many of the veins and arteries running throughout the human body were found and the directions in which they traveled. Doctors of this time realized if these were plugged, blood could not continue to flow out of the body. Nevertheless it took until the invention of the printing press during the fifteenth century for medical notes and ideas to travel westward, allowing for the idea and practice of Hemostasis to be expanded.[12]

Hemostatic Research

There is currently a lot of research being conducted on hemostasis. The most current research is based on genetic factors of hemostasis and how it can be altered to reduce the cause of genetic disorders that alter the natural process hemostasis.[13]

Von Willebrand disease is associated with a defect in the ability of the body to create the platelet plug and the fibrin mesh that ultimately stops the bleeding. New research is concluding that the von Willebrand disease is much more common in adolescence. This disease negatively hinders the natural process of Hemostasis causing excessive bleeding to be a concern in patients with this disease. There are complex treatments that can be done including a combination of therapies, estrogen-progesterone preparations, desmopressin, and Von Willebrand factor concentrates. Current research is trying to find better ways to deal with this disease; however, much more research is needed in order to find out the effectiveness of the current treatments and if there are more operative ways to treat this disease.[14]


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  2. ^ Boon, G. D. "An Overview of Hemostasis." Toxicologic Pathology 21.2 (1993): 170-79.
  3. ^ a b Clemetson, Kenneth J. "Platelets And Primary Haemostasis." Thrombosis Research 129.3 (2012): 220-224 http://www.sciencedirect.com/science/article/pii/S0049384811006323
  4. ^ Lassila, Riitta (2012). "New Insights Into Von Willebrand Disease And Platelet Function". Seminars In Thrombosis & Hemostasis 38.1: 55–63.
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  7. ^ Aldo Moraci, et al. "The Use Of Local Agents: Bone Wax, Gelatin, Collagen, Oxidized Cellulose." European Spine Journal 13.(2004): S89-S96.
  8. ^ Smith, Shondra L., John M. Belmont, and J. Michael Casparian. "Analysis Of Pressure Achieved By Various Materials Used For Pressure Dressings." Dermatologic Surgery 25.12 (1999): 931-934.
  9. ^ Orhan Kozak, et al. "A New Method For Hepatic Resection And Hemostasis: Absorbable Plaque And Suture." Eurasian Journal Of Medicine 41.(2010): 1-4. Academic Search Complete.
  10. ^ Mohammadreza Tahriri, et al. "Preparation And Characterization Of Absorbable Hemostat Crosslinked Gelatin Sponges For Surgical Applications." Current Applied Physics 11.3 (2011): 457-461.
  11. ^ Tocantins, 1Leandro M.; Reid, William O.; Silver, Melvin J.; Kazal, Louis A. (1964). "Current Problems In Hemostasis". Annals of the New York Academy of Sciences 115.2 Computers: 21–30. doi:10.1111/j.1749-6632.1964.tb41028.x. http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1964.tb41028.x/abstract. Retrieved 29 April 2012.
  12. ^ "Wies, C. H. "The History of Hemostasis." Yale Journal of Biology and Medicine 2". 1929. pp. 167–68. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2606227/.
  13. ^ "Rosen, E. D., Xuei, X., Suckow, M., & Edenberg, H. (2006). Searching for hemostatic modifier genes affecting the phenotype of mice with very low levels of FVII. Blood Cells, Molecules & Diseases, 36(2), 131-134. doi:10.1016/j.bcmd.2005.12.037". http://web.ebscohost.com/ehost/detail?vid=15&hid=122&sid=0e0b482d-9979-42b7-8837-e409e9a1fa1e%40sessionmgr114&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=a9h&AN=20252929.
  14. ^ Mikhail, S.; Kouides, P (2010). "von Willebrand Disease in the Pediatric and Adolescent Population". Journal Of Pediatric & Adolescent Gynecology 23: S3-S10. doi:10.1016/j.jpag.2010.08.005. http://web.ebscohost.com/ehost/detail?vid=13&hid=122&sid=0e0b482d-9979-42b7-8837-e409e9a1fa1e%40sessionmgr114&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=a9h&AN=55091303.

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